hif-1α与vegf在大鼠缺血缺氧性脑损伤中的表达分析

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1、中文摘要3HIF．1a只在一定氧浓度范围内表达，梗塞中心区完全缺氧情况下，神经元坏死后则无表达；缺血半暗区存在一定程度缺氧，HIF．1a在此处的神经元中存在明显高表达。4HIF．1a与VEGF于缺血梗塞24h时蛋白表达水平达到高峰，随梗塞时间的延长其表达水平呈峰样变化。5在缺血梗塞后，HIF．1a与VEGF在脑组织中的表达水平随时间变化表现出升降一致的特点，二者的表达之间具有明显的相关性。关键词：动物模型；脑缺血；缺氧诱导因子．10【；血管内皮生长因子英文摘要一_一—————————_—————————_—^————————————————————————————

2、———————_————一TheexperimentalstudyonexpressionofHIF··laandVEGFinratswithhypoxic--ischemicbraindamageABSTRACTCerebralStrokeisaverycommonfataldiseaseinnervoussystem．Itthreatenshuman’Shealthwithitshighattackrate，disabilityrateandcasefatalityrate．AndischemicCerebralStrokeoccupiesabout60．80

3、％ofthetotal．Sometherapiesincludethrombolysisandcraniotomyareeffectivetofewpatientsatpresent．Therefore，it’Simminenttoilluminatethemolecularmechanismandfindanewtherapeuticregimen．objective：Thisexperimentalstudyisforpreparingaratmodelwithpermanentmiddlecerebralarteryocclusion(MCAO)andest

4、imatingthemodelbyusingthefollowingmethodsas：ethologyscoreofthelossofneuralfunction，determiningthe‘nfaretithroughTTCstaininobservingtheinfarctionscopetlarougnstaining,oDserVmghistopathologyandultramicrostructureoftherat’sbraintissues，andforfindingthetheoryevidenceofeffectivetreatmentby

5、detectingtheexpressionofHIF—laandVEGFintheexperimentalischemicbraintissuesandobservingtheregularityofexpressionandmolecularmechanism．Methods：lAnimalsandgroups：Atotalof80healthyadultSprague．Dawleyrats，weighting250—2809，randomlydivided5英文摘要into3groups：normalcontrolgroup(n=5)，experimentg

6、roup(n-50)，andshamoperatedgroup(n=25)．Theexperimentgroupandtheshamoperatedgroupdividedinto5subgroupsbydifferentinfarctiontime：6h，12h，24h，72h，7d．2Modelpreparation：Preparetheratmodelwithpermanentmiddlecerebralarteryocclusion(MCAO)usingintraluminalsuturebyZeaLonga’Smethod．Theoperationste

7、pofshamoperatedgroupwassameasexperimentgroupexceptforpluggingthesutureincarotidartery．Allratswereestimatedbyethologyscoreofthelossofneuralfunctionafteroperation．Theanimalswhosescorefrom1-3wereselectedtoexperimentgroup．3Animalsineachgroupwerekilledatdifferentpresettime，andthebrainswere

8、colle